Steady state levels of the mRNAs for alpha1B, beta1 and beta2-adrenergic receptors (alpha1B-AR, beta1AR, beta2AR) were quantified by DNA excess solution hybridization assays in the heart, lungs and liver of rats. Tissues for RNA extraction were obtained from euthyroid and thyroidectomized rats and from thyroidectomized rats treated with a single dose of thyroxine. Thyroidectomy resulted in significant decreases in beta1AR and beta2AR mRNAs in heart and lung and alpha1B-AR mRNA in liver, whereas the levels of beta2AR mRNA in liver and alpha1B-AR mRNA in lung and heart were significantly increased. All these changes were reversed within 20 hours of a single s.c injection of 1 mg/kg thyroxine. These findings indicate for the first time that thyroid state regulates mRNA levels for adrenergic receptors, and that this regulation is tissue- and receptor-specific. The changes in adrenergic receptor mRNAs correlate with and probably underlie the well documented, thyroid-dependent changes in the cellular densities and physiological reactivities of adrenergic receptors. Steady state levels of alpha1B-AR and beta2AR mRNAs were also quantified in freshly isolated rat hepatocytes and in hepatocytes incubated in vitro in Krebs buffer for 2-24 hr. A significant decrease in alpha1B-AR mRNA and a parallel increase in beta2AR mRNA was detected as early as after 2 hr of incubation of cells. These changes precede and are probably related to the well documented time-dependent conversion from `1- to a2-adrenergic glycogenolysis in isolated hepatocytes.